Glaucoma is an ocular disorder characterized in that it is a neuropathy in which several mechanisms causing damage and loss of retinal ganglion cells intervene, one of the main factors and to date a controllable factor is that of intraocular pressure, and an objective of the disclosure is to keep the intraocular pressure at a normal level. One of the theories is that cell damage is caused by the elevated intraocular pressure that by means of mechanical action causes compression of the nervous fibers and consequently damage to the optical nerve, which is expected to gradually lead to irreversible damage to ganglion cells, nervous fibers and atrophy of the optical nerve and consequently damage and visual field loss until eyesight is lost completely.
The frontal part of the eye is filled with a clear liquid called aqueous humor, which is primarily produced in the ciliary passages found behind the iris. This liquid exits or is removed from the eye through canals in the frontal part thereof, in an area called the anterior chamber angle, at times simply referred to as “angle.”
A normal eye has been generally considered as having a normally appropriate intraocular pressure of about 10 to about 20 mm Hg, through the circulation inside the aqueous humor of the eye, which is secreted from the ciliary body, goes through the pupil to the anterior chamber of the eyeball, and is filtered outside the eyeball through the trabecular meshwork and the Schlemm's canal. When the aqueous humor excreting passageway is blocked, the aqueous humor cannot leave the eyeball at a suitable speed, the intraocular pressure is increased, the eyeball hardens, and direct damage is produced, subsequently developing atrophy of the optical nerve, which is called glaucoma. A characteristic optical neuropathy is developed, resulting in progressive loss of ganglion cells of the retina, visual field restriction, and finally producing blindness. The advanced stages of the illness are also characterized by significant pain.
Treatment for glaucoma, if started early in the course of the illness, may avoid additional damage and preserve the most of the ocular functions. The object of glaucoma treatment is to reduce the intraocular pressure until reaching a level considered safe particularly for the sight, but which is not so low as to cause an ocular malfunction or retinal complications.
There are diverse and varied techniques for treating intraocular high pressure “deviating” the aqueous humor to adjacent tissues contained inside the eyeball, all beneath the sclera or conjunctiva, this technique being subject to the ability of absorbing each one of the tissues wherein the liquid causing the elevated intraocular pressure is canalized.
Typical ophthalmic implants have a valve mechanism to regulate the aqueous humor flow from the anterior chamber; defects in and/or failure of said valve mechanisms can lead to an excessive loss of aqueous humor from the eyeball and possible hypotony. The implants also tend to be obstructed as time goes by, whether from the interior by the tissue, such as the iris, being inhaled at the entrance, or from the exterior by cell proliferation, for example, by forming scars. Furthermore, typical operation of inserting the implant is complicated, highly traumatic and takes a long time.
U.S. Pat. No. 3,788,327 shows an implant from the state of the art using a valve mechanism for regulating the aqueous humor flow from the eyeball to its exterior.
The deficiency and main drawback of this device is the existence of a gap or cavity between the upper part of its liquid-releasing mechanism and the output hole located in the exterior of the eye that is directly connected to the environment and eyelids; since said cavity is highly inclined to organic and inorganic matter sedimentation that will restrict or impede free movement of the release mechanism and/or will generate an obstruction (clogging) in the aqueous humor exit channel, thus resulting in deficiency of its performance and draining capacity of aqueous humor and increasing the intraocular pressure.
The functioning of this device and draining capacity is unsafe since it is conditioned to free movement in its release mechanism, free fluid conduction and the lack of obstacles in the channel removing the aqueous humor towards the outside of the eye and does not have any mechanism nor measures to impede forming these restrictions and/or obstructions.
Another drawback or deficiency of this device results in its high feasibility of establishing bacterial colonies in the cavity existing between the upper part of its liquid release mechanism and the output hole located outside the eye, since this channel does not have any mechanism or measure to impede the formation and accumulation of bacteria as well as the eye's own secretions.
This device has a high endophtalmitis risk, since clogging the channel existing in the upper part of the release mechanism will cause an aqueous humor blockage in its inside, and thus bacteria will find here a favorable niche for its rapid development and entrance to the inside of the eye.
As previously mentioned, the defects and/or failure in the mechanism and drainage of the valve could lead to increasing the intraocular pressure.
The device of the present disclosure does not depend on the capacity of absorption of any tissue to remove the aqueous humor without obstructions between its spindle and the outside. Also, its implant process is the least traumatic possible, typically requiring only ambulatory or out-patient surgery, the device or valve of the disclosure being based on its design simplicity and components. The present valve comprises an interior part or chassis and a stem that is displaced outside in the corneal surface (over the epithelium), the valve stem is subject to a tension caused by a compression spring or the repulsion between two permanent magnets, this spring or the magnetic repulsion are calibrated to a given tension (about 10 to about 20 mm Hg), and when the eyeball reaches the tension value greater than the spring or the repulsion, it achieves displacement of the stem outside the cornea, such that the aqueous humor causing the elevated intraocular pressure can be drained outside the eye. Once the pressure is regulated, the stem returns to its initial position tightly closing the valve and thus avoiding any entrance of foreign objects, such as dust, microorganisms, etc., into the eye.
There are very clear and precise advantages between the device of the present disclosure and the devices from the state of the art. These include:                Regulating pressure is always constant, and the aqueous humor flow is free of obstacles.        The smooth exterior upper surface of the device allows cleaning and constant lubrication through the natural movement of the eyelids impeding formation of sediments and bacteria build-up.        The lack of interior and exterior cavities impedes the formation of sediments and bacteria build-up.        The drainage mechanism is always free and lacks movement restrictions; thus its functioning does not have conditions.        This type of configuration allows a laminar flow of the aqueous humor through the device walls to achieve a sweeping effect and thus avoid adherence of bacterial strains.        
The present disclosure provides an intraocular pressure compensating and regulating valve installed on the cornea of an eye, comprising: a valve body having a valve seat on one end; a mobile element in contact with the valve seat under normal intraocular pressure conditions in the eye; the mobile element is configured such that it can be separated from the valve seat when the intraocular pressure exceeds an intraocular pressure limit; and an element is provided to keep the mobile element in contact with the valve seat. The valve body has an exterior part with fastening elements to retain the valve to the cornea, and the intraocular pressure limit is from about 10 to about 20 mm Hg.
In a first embodiment, the element to keep the mobile element in contact with the valve seat is a spring placed on an interior part of the valve body, and the mobile element is a stem comprising a tubular body with an internal canal therein, the stem having on its upper part perforations for allowing the aqueous humor exit the valve.
In a second embodiment, the element to keep the mobile element in contact with the valve seat is constituted by two permanent magnets with the same polarity placed on an interior part of the valve part, and the mobile element is a stem comprising a tubular body with an internal canal therein, the stem having on its upper part perforations for allowing the aqueous humor exit the valve.
In a third embodiment, the mobile element is a stem comprising a tubular body with an internal canal therein, and the element for keeping the mobile element in contact with the valve seat is constituted by two springs placed in contact with one valve body end opposite the end where the valve seat is and a ring located in the stem, the stem having on its upper part perforations for allowing the aqueous humor exit the valve.
In a fourth embodiment, the element to keep the mobile element in contact with the valve seat is a spring having a first end and a second end, the spring is located in an interior part of the valve body, and the mobile element is a pad having on its lower part a hoop to fasten a first end of the spring; and the second end of the spring is attached to a fastening element located on the inside part of the valve body.